Bile acids play a key role in fat absorption. Fifty percent of calories ingested by infants are fat calories. Previous studies have established that certain of the mechanisms of bile acid transport and metabolism are immature in the near-term fetus and newborn. This is a contributory factor to the steatorrhea evident in low-birth weight infants. During the present period of grant support, several aspects of fetal and neonatal bile acid metabolism are under investigation. Neonatal intestinal bile active transport, its development during the neonatal period, and the control of its onset of activity are being examined. The rate of development of fetal hepatic bile acid secretion and the control of onset of secretion are being studied. The metabolic pathways for bile acid synthesis and, specifically, certain "aberrant" feto-maternal synthetic pathways are under investigation. Information is being developed to define the condition best characterized as neonatal "physiologic cholestasis." It is evident that the hepatic secretory apparatus in otherwise normal low-birth weight infants is "defective." This defect, which is only now gaining general recognition, is comparable to the better known developmental defect of bilirubin metabolism called "physiologic jaundice."